Molecular mechanism of pancreatic alpha cell failure in type 2 diabetes
| Project/Area Number |
25293208
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Metabolomics
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| Research Institution | Gunma University |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥18,460,000 (Direct Cost: ¥14,200,000、Indirect Cost: ¥4,260,000)
Fiscal Year 2015: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥7,800,000 (Direct Cost: ¥6,000,000、Indirect Cost: ¥1,800,000)
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| Keywords | グルカゴン / Sirt1 / 膵α細胞 / 糖尿病 / α細胞 / FoxO1 / ATF3 |
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| Outline of Final Research Achievements |
Pancreatic alpha cell dysfunction as well as beta cell dysfunction is known to be important for pathophysiology of type 2 diabetes. However, its molecular mechanism has been unclear. Thus, we generated both knockout mice and knockin mice in which Sirt1, an NAD-dependent deacetylase and a cellular energy sensor, lack or overexpress specifically in alpha cells. The metabolic profiles and histological analysis revealed that Sirt1 negatively regulates alpha cell differentiation/proliferation, and positively regulates glucose-dependent glucagon secretion.
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Report
(4 results)
Research Products
(1 results)
